Evidence map›Paper›PMID 41046979›Full record

ReviewMolecules and cells2025

Dual SMAD inhibition as a versatile platform in human pluripotent stem cell-based regenerative medicine and disease modeling.

Lesly Puspita, Magdalena Deline, Jae-Won Shim

Abstract readReview
In one paragraph

Review in Molecules and cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Lesly PuspitaSoonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si 31151, Korea.
Magdalena DelineSoonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si 31151, Korea; Department of Integrated Biomedical Science, Soonchunhyang University, Cheonan-si 31151, Korea.
Jae-Won ShimSoonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si 31151, Korea; Department of Integrated Biomedical Science, Soonchunhyang University, Cheonan-si 31151, Korea. Electronic address: shimj@sch.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dual SMAD inhibition is a robust and widely adopted protocol for directing human pluripotent stem cells (hPSCs) toward neuronal lineages by blocking transforming growth factor-beta and bone morphogenetic protein pathways. Suppressing transforming growth factor-beta and bone morphogenetic protein signaling enables efficient and reproducible induction of neuroectoderm, serving as the foundation for generating diverse brain region-specific neuronal subtypes. This review outlines the mechanistic basis and major achievements of the dual SMAD inhibition strategy, including its application in 2 recent clinical trials for Parkinson's disease, and its role in preclinical studies targeting conditions, such as spinal cord injury (SCI), retinal degeneration, and amyotrophic lateral sclerosis (ALS). In addition to its significant contribution to the generation of transplantation-ready grafts from hPSCs, the protocol serves as a valuable platform for disease modeling across various neurological and metabolic disorders. The key strengths include high efficiency, technical simplicity that enables precise control of cell fate using small molecules, versatility in both 2- and 3-dimensional culture systems, and reproducibility across various hPSC lines. This review also addresses key limitations, such as restricted gliogenic capacity and limited neural progenitor cell expansion. Future research should focus on incorporating emerging technologies to advance stem cell-based applications. Overall, dual SMAD inhibition represents a powerful and versatile platform for stem cell-based neuroscience and regenerative medicine.

Indexed as

Pluripotent Stem CellsRegenerative MedicineSmad ProteinsAnimalsCell DifferentiationHumansSignal TransductionSmad ProteinsDisease modelingHuman pluripotent stem cellsNeuronal differentiationRegenerative medicineSignal pathway

Identifiers

PMID41046979
PMCPMC12581692

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.